Effects of dietary fiber and protein concentration on growth, feed efficiency, visceral organ weights and large intestine microbial populations of swine

Finishing barrows (average initial weight 55.5 +/- 2.4 kg) were used to determine the effects of high dietary fiber or protein on performance, visceral organ weights and large intestine microbial populations and to monitor the duration of regression of swine visceral organ mass and microbial populations to control values following transfer from the high fiber or high protein diet to the control diet. Four pigs from each diet were killed on d 17, 34, 48 and 66. From d 34 until slaughter 14 and 32 d later, all remaining pigs were fed the control diet ad libitum. High fiber resulted in significantly higher relative weight of the total gastrointestinal tract after 34 d and higher relative stomach weight up to d 48. Compared with the control diet, the high protein diet resulted in increased relative liver and kidney weights up to d 48. The number of proteolytic and cellulolytic bacteria increased in the colon contents of pigs fed a high protein or high fiber diet, respectively, but declined to below control values within 14 d of transferring pigs from the high protein or high fiber diet to the control diet. The results indicate that diet composition plays a more specific role in visceral organ hypertrophy than can be explained by the normal relative changes in organ size as body weight increases. Thus, high dietary fiber and protein may indirectly increase the animal's maintenance requirement by causing a repartitioning of nutrients from the edible carcass to the visceral organs.     

Update: dietary protein and microbial protein contribution

Factors influencing microbial protein synthesis in the rumen have been reviewed several times in recent years. Original publications in the past 3 yr have reported microbial and feed protein nitrogen contribution postruminally when feeding a variety of dietary proteins. Ammonia is a satisfactory source of nitrogen for growth of the majority of rumen species, but substitution of intact protein for urea (source of ammonia) usually stimulates microbial protein production. Protein sources such as soybean meal appear to possess properties (perhaps rate of degradability) that optimize microbial growth in vivo. Protein sources more undegradable than soybean meal, when fed as the major nitrogen source, sometimes reduce microbial growth. However, nondegradable proteins may compensate for less microbial protein by supplying intact dietary protein postruminally, so the amino acids potentially available may be equal to or greater than those available when readily degradable protein is fed. Soybean meal may reduce microbial growth in diets containing grass silage at protein exceeding 16.8%. Various measurements of microbial and intact dietary protein postruminally show that the contribution of each can be manipulated. Accuracy of quantitative predictions of postruminal contribution depends on several factors that require more research.     

Evaluation of phage treatment as a strategy to reduce Salmonella populations in growing swine

Salmonella is a foodborne pathogenic bacterium that causes human illnesses and morbidity and mortality in swine. Bacteriophages are viruses that prey on bacteria and are naturally found in many microbial environments, including the gut of food animals, and have been suggested as a potential intervention strategy to reduce Salmonella levels in the live animal. The present study was designed to determine if anti-Salmonella phages isolated from the feces of commercial finishing swine could reduce gastrointestinal populations of the foodborne pathogen Salmonella Typhimurium in artificially inoculated swine. Weaned pigs (n?=?48) were randomly assigned to two treatment groups (control or phage-treated). Each pig was inoculated with Salmonella Typhimurium (2?×?10(10) colony forming units/pig) via oral gavage at 0?h and fecal samples were collected every 24?h. Swine were inoculated with a phage cocktail via oral gavage (3?×?10(9) plaque forming units) at 24 and 48?h. Pigs were humanely killed at 96?h, and cecal and rectal intestinal contents were collected for quantitative and qualitative analysis. Fecal Salmonella populations in phage-treated pigs were lower (p?1.4?log(10) colony forming units/g digesta, and rectal populations were numerically reduced. The number of pigs that contained inoculated Salmonella Typhimurium was reduced by phage treatment, but a significant (p?相似文献   

The science of muscle hypertrophy: making dietary protein count

Growing evidence supports the conclusion that consumption of protein in close temporal proximity to the performance of resistance exercise promotes greater muscular hypertrophy. We can also state with good certainty that merely consuming energy, as carbohydrate for example, is also not sufficient to maximise muscle protein synthesis leading to anabolism and net new muscle protein accretion. Recent work also indicates that certain types of proteins, particular those that are rapidly digested and high in leucine content (i.e. whey protein), appear to be more efficient at stimulating muscle protein synthesis. Continued practice of consumption of these types or proteins after exercise should lead to greater hypertrophy. Reviews of numerous training studies indicate that studies in which milk proteins and principally whey protein show an advantage of these proteins over and above isoenergetic carbohydrate and soya protein in promoting hypertrophy. Thus, the combined evidence suggests a strategic advantage of practising early post-exercise consumption of whey protein or dairy-based protein to promote muscle protein synthesis, net muscle protein accretion and ultimately hypertrophy.     

Lipoprotein lipid and protein responses to dietary fat and diabetes in rats

Dietary and insulin-deficiency types of hyperlipidemia were compared in adult normal and streptozotocin-induced diabetic male breeder rats. High beef tallow, high corn oil or low fat diets (BT, CO and LF, respectively) were fed ad libitum for 2 months. Glucose and insulin were measured in plasma and total cholesterol, free cholesterol, cholesteryl ester, triglycerides and apoproteins in very low density, low density and high density lipoproteins (VLDL, LDL and HDL, respectively). Diet did not affect plasma glucose or insulin levels. LDL-triglycerides were higher in BT and diabetic than in CO and LF rats. HDL-free cholesterol levels were higher in CO- and LF-than in BT-fed rats. Diabetes resulted in a decrease in HDL-cholesterol. Diabetic animals had higher HDL-apoA-I (apolipoprotein A-I) levels than did CO- and LF- but not BT-fed rats. VLDL-triglycerides were higher in diabetic than in normal rats, with no dietary differences in normal rats. In LDL, apoB levels were lower and apoE levels were higher in LF-fed rats than in animals fed high fat diets. Diabetes resulted in an increase in LDL-apoB but a decrease in LDL-apoE. HDL-apoE levels were higher, although HDL-apoA-I levels were lower in LF than in high fat-fed rats. The results related to lipoprotein composition supported the hypothesis that excess intake of a diet high in saturated fat may contribute to a metabolic pattern that resembles that of a diabetic state.     

Skeletal muscle responses to negative energy balance: effects of dietary protein

Sustained periods of negative energy balance decrease body mass due to losses of both fat and skeletal muscle mass. Decreases in skeletal muscle mass are associated with a myriad of negative consequences, including suppressed basal metabolic rate, decreased protein turnover, decreased physical performance, and increased risk of injury. Decreases in skeletal muscle mass in response to negative energy balance are due to imbalanced rates of muscle protein synthesis and degradation. However, the underlying physiological mechanisms contributing to the loss of skeletal muscle during energy deprivation are not well described. Recent studies have demonstrated that consuming dietary protein at levels above the current recommended dietary allowance (0.8 g · kg(-1) · d(-1)) may attenuate the loss of skeletal muscle mass by affecting the intracellular regulation of muscle anabolism and proteolysis. However, the specific mechanism by which increased dietary protein spares skeletal muscle through enhanced molecular control of muscle protein metabolism has not been elucidated. This article reviews the available literature related to the effects of negative energy balance on skeletal muscle mass, highlighting investigations that assessed the influence of varying levels of dietary protein on skeletal muscle protein metabolism. Further, the molecular mechanisms that may contribute to the regulation of skeletal muscle mass in response to negative energy balance and alterations in dietary protein level are described.     

Effect of low-quality dietary protein on the thymus of growing rats

The status of the thymus of growing rats fed for 45 days after weaning on a low-quality dietary protein (7.5% maize) was compared with that in an age-matched control group receiving a diet containing casein at the same concentration. At the end of the feeding period, body weight (bw) was determined and the thymus was removed; its weight and cell number and the mature T-cell population--characterized by the monoclonal antibody W3/13 using the indirect immunofluorescence technique--were determined. Thymus weight expressed as mg/bw0.75 (3.9 +/- 0.75 vs 7.7 +/- 2.0), cell number (4.4 +/- 2.2 vs 26.3 +/- 7.6), and the absolute number of W3/13+ T cells (1.59 +/- 0.75 vs 17.8 +/- 5.4) were significantly lower (p less than 0.0005) in the experimental group than in the control group. The results suggest severe atrophy of the thymus of weaning animals chronically fed a low-quality protein.     

Metabolic epidemiology of colon cancer: dietary pattern and fecal sterol concentrations of three populations

The nutrient intake, fecal neutral sterol concentration, and bile acid concentration of populations with a varied risk for colon cancer development were investigated. High-risk populations in the metropolitan New York area and Malmo, Sweden, were compared with an intermediate-risk population in Umea, Sweden. The mean daily intake of protein and fat was comparable in all groups, but the total daily fiber intake was higher in Umea, as was the total daily stool output. There was no difference in the total fiber intake and stool output between Malmo and metropolitan New York. The fecal secondary bile acid concentration was lower in Umea than in the other two areas; no difference was observed between Malmo and metropolitan New York. These results suggest that high fiber intake may be considered protective against colon cancer even in a population with a high risk intake. A high dietary fiber intake may limit colon cancer risk by increasing stool bulk, and thus diluting and/or binding tumor promoters.     

Further researches about retinal damages and dietary protein imbalance in growing rats.

Following previous trials about hypo- and hyper-protein diets and their negative effects on some ocular structures when administered in selected stages of rats' growth, Authors have presented a comparative study of retinal alterations between light (LM) and electron (EM) microscopic analysis. LM showed a vacuolar degeneration of retinal optic fiber and ganglion cell layers where EM, performed at the same time, showed damages of the nervous tissue consisting of microtubule diminution, optic fiber molding and glial cell proliferation.     

Sulfur amino acid requirements of the growing rat fed eight percent dietary protein

Methionine and methionine plus cystine requirements of the growing rat fed equivalent to 8% dietary protein were determined. Diets formulated to be adequate in all nutrients except sulfur amino acids (SAA) and providing 4% protein from ANRC casein and equivalent to 4% casein protein from amino acids (excluding methionine and cystine) were supplemented with graded levels of L-methionine. The diet providing 0.34% total SAA (0.32% L-methionine + 0.02% L-cystine) gave the best feed/gain ratio, relative net protein ratio (RNPR), liver protein utilization (LPU) and plasma amino acid acid parameters. When similar ANRC casein + crystalline amino acid diets providing 0.44% total SAA but varying in ratio (by weight) by methionine/cystine were fed to rats, optimal feed/gain ratio, RNPR and plasma amino acid parameters were obtained when cystine replaced 33 to 60% of dietary L-methionine. Inclusion of L-cystine at the expense of L-methionine in these 8% protein diets improved overall rat performance and utilization of dietary methionine. Supplementation of the casein + amino acid basal diet with methionine sulfoxide, methionine sulfone (oxidized forms of methionine) or cysteic acid (oxidized form of cysteine/cystine) to provide 0.34% total SAA, indicated that relative to methionine (100), methionine sulfoxide was completely available and methionine sulfone (68) and cysteic acid (55) were less available. Correction for methionine and cystine digestibilities in ANRC casein suggests that the SAA requirements for the growing rat are 0.33% of diet or 4.1% of dietary protein when 8% protein diets are fed.     

Association between low colonic short-chain fatty acids and high bile acids in high colon cancer risk populations

We propose that the influence of diet on colon cancer risk is mediated by the microbiota. To investigate how dietary fat influences risk, we compared the colonic contents of 12 adult high-risk African Americans (AAs) and 10 Caucasian Americans (CAs) who consumed a high-fat diet (123 ± 11 g/d and 129 ± 17 g/d, respectively) to 13 native Africans (NAs) who subsisted on a low-fat (38 ± 3.0 g/d) diet, all aged 50-60 yr. The colonic bile acids were measured by LC-MS and the short-chain fatty acids (SCFAs) by GC. The chief secondary colonic bile acids, deoxycholic acid and lithocholic acid, were correlated with fat intake and similar between AAs and CAs, but 3-4 times higher than in AAs (p < 0.05). The major SCFAs were lower in AAs (p < 0.001) and CAs (p < 0.001) compared to AAs, but conversely, the branched chain fatty acids (BFCA) were higher. Our results suggest that the higher risk of colon cancer in Americans may be partly explained by their high-fat and high-protein, low complex carbohydrate diet, which produces colonic residues that promote microbes to produce potentially carcinogenic secondary bile acids and less antineoplastic SCFAs. The role of BCFA in colonic carcinogenesis deserves further study.